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Date: | Mon, 23 Apr 2018 12:58:30 +0000 |
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I found an explanation in
Pang, Hartman J Mammary Gland Biol Neoplasia 2007 12:211-221 'Initiation of Human Lactation: Secretory Differentiation and Secretory Activation:
'Glucocorticoid receptors are present in the cytosol of
mammary epithelial cells and when bound to glucocorticoids,
the receptors translocate to the nucleus and act
synergistically with prolactin-activated transcription factors
to enable the synthesis of milk proteins, such as, casein and
α-lactalbumin. While progesterone binds to the glucocorticoid
receptor, it does not then translocate to the nucleus
and activate the milk protein genes [49]. Although the
affinity of the binding of progesterone to the glucocorticoid
receptor is lower than that of the glucocorticoids, the free
concentrations of progesterone are much higher than the
glucocorticoids during pregnancy [9, 61–63]. Thus progesterone
may displace the glucocorticoids binding from the
glucocorticoid receptor during pregnancy. This competition
for the glucocorticoid receptor may ensure that secretion
from the mammary gland is minimal as it develops its
secretory capacity during pregnancy. On the other hand,
others have concluded that the progesterone receptor itself is
responsible for progesterone’s inhibition of milk synthesis
during pregnancy.
In other words, the progesterone is binding to glucocorticoid receptors, not PRL receptors. When progesterone is bound to these receptors, PRL-activated transcription factors cannot enable the synthesis of milk proteins, which is crucial to make milk.
Anne
Anne Eglash MD, IBCLC, FABM
Clinical Professor, Department of Family and Community Medicine
University of Wisconsin School of Medicine and Public Health
Medical Director, UW Lactation Services
Medical Director, Mothers Milk Bank of the Western Great Lakes
Founder and President of The Milk Mob, dedicated to building Breastfeeding Knowledgeable Medical Systems and Communities http://www.themilkmob.org
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